Evidence map›Paper›PMID 23755094›Full record

ArticlePloS one2014

Müller cell reactivity in response to photoreceptor degeneration in rats with defective polycystin-2.

Stefanie Vogler, Thomas Pannicke, Margrit Hollborn, Antje Grosche, Stephanie Busch, Sigrid Hoffmann, Peter Wiedemann, Andreas Reichenbach, Hans-Peter Hammes, Andreas Bringmann

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.5field-weighted citation impact, top 19% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 26 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 1 country.

Stefanie VoglerPaul Flechsig Institute of Brain Research, University of Leipzig, Leipzig, Germany.
Thomas Pannicke
Margrit Hollborn
Antje Grosche
Stephanie Busch
Sigrid Hoffmann
Peter Wiedemann
Andreas Reichenbach
Hans-Peter Hammes
Andreas Bringmann
Leipzig University · DEUniversity Hospital Leipzig · DEUniversity Medical Centre Mannheim · DEHeidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRetinal degeneration in transgenic rats that express a mutant cilia gene polycystin-2 (CMV-PKD2(1/703)HA) is characterized by initial photoreceptor degeneration and glial activation, followed by vasoregression and neuronal degeneration (Feng et al., 2009, PLoS One 4: e7328). It is unknown whether glial activation contributes to neurovascular degeneration after photoreceptor degeneration. We characterized the reactivity of Müller glial cells in retinas of rats that express defective polycystin-2.

methodsAge-matched Sprague-Dawley rats served as control. Retinal slices were immunostained for intermediate filaments, the potassium channel Kir4.1, and aquaporins 1 and 4. The potassium conductance of isolated Müller cells was recorded by whole-cell patch clamping. The osmotic swelling characteristics of Müller cells were determined by superfusion of retinal slices with a hypoosmotic solution.

findingsMüller cells in retinas of transgenic rats displayed upregulation of GFAP and nestin which was not observed in control cells. Whereas aquaporin-1 labeling of photoreceptor cells disappeared along with the degeneration of the cells, aquaporin-1 emerged in glial cells in the inner retina of transgenic rats. Aquaporin-4 was upregulated around degenerating photoreceptor cells. There was an age-dependent redistribution of Kir4.1 in retinas of transgenic rats, with a more even distribution along glial membranes and a downregulation of perivascular Kir4.1. Müller cells of transgenic rats displayed a slight decrease in their Kir conductance as compared to control. Müller cells in retinal tissues from transgenic rats swelled immediately under hypoosmotic stress; this was not observed in control cells. Osmotic swelling was induced by oxidative-nitrosative stress, mitochondrial dysfunction, and inflammatory lipid mediators.

interpretationCellular swelling suggests that the rapid water transport through Müller cells in response to osmotic stress is altered as compared to control. The dislocation of Kir4.1 will disturb the retinal potassium and water homeostasis, and osmotic generation of free radicals and inflammatory lipids may contribute to neurovascular injury.

Indexed as

AgingAnimalsAquaporin 1Aquaporin 4Cell MembraneCell SeparationEpendymoglial CellsGene Expression RegulationGlial Fibrillary Acidic ProteinGlutamate-Ammonia LigaseInflammation MediatorsIntermediate FilamentsNestinOsmosisOxidative StressPhotoreceptor Cells, VertebrateAquaporin 1Aquaporin 4Glial Fibrillary Acidic ProteinGlutamate-Ammonia LigaseInflammation MediatorsNestinPotassium Channels, Inwardly RectifyingTRPP Cation ChannelsVimentin

Identifiers

PMID23755094
PMCPMC3670868
OpenAlexW1977144362

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.